Multiple roles of STAT3 in cardiovascular inflammatory responses

Prog Mol Biol Transl Sci. 2012:106:63-73. doi: 10.1016/B978-0-12-396456-4.00010-9.

Abstract

Cardiovascular inflammation has been regarded as a major cause for heart failure. However, the mechanisms that are involved in the regulation of cardiovascular inflammation are not well understood. In this chapter, we review the recent progress in revealing the roles of STAT3 in cardiovascular inflammation. Particularly, we discuss cardiomyocyte-specific STAT3-deficient mice and their phenotypes. An emerging view is that STAT3 plays a key role not only in cardiac protection but also in the control of cardiac-related inflammation.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / metabolism
  • Cardiovascular Diseases / physiopathology*
  • Cytokine Receptor gp130 / physiology
  • Cytokines / physiology
  • Endothelial Cells / metabolism
  • Gene Expression Regulation
  • Heart Failure / etiology
  • Heart Failure / physiopathology
  • Humans
  • Inflammation
  • Interleukin-6 / physiology
  • Mice
  • Mice, Transgenic
  • Models, Cardiovascular
  • Myocardial Ischemia / physiopathology
  • Myocytes, Cardiac / metabolism
  • Phosphoproteins / metabolism
  • Phosphorylation
  • Protein Processing, Post-Translational
  • Rats
  • STAT3 Transcription Factor / deficiency
  • STAT3 Transcription Factor / genetics*
  • STAT3 Transcription Factor / physiology*
  • Signal Transduction

Substances

  • Cytokines
  • IL6ST protein, human
  • Interleukin-6
  • Phosphoproteins
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Stat3 protein, mouse
  • Cytokine Receptor gp130